TY - JOUR
T1 - Proinflammatory T cell status associated with early life adversity
AU - Elwenspoek, Martha M.C.
AU - Hengesch, Xenia
AU - Leenen, Fleur A.D.
AU - Schritz, Anna
AU - Sias, Krystel
AU - Schaan, Violetta K.
AU - Mériaux, Sophie B.
AU - Schmitz, Stephanie
AU - Bonnemberger, Fanny
AU - Schächinger, Hartmut
AU - Vögele, Claus
AU - Turner, Jonathan D.
AU - Muller, Claude P.
N1 - Funding Information:
This work was supported by Luxembourg National Research Fund Grant C12/BM/ 3985792 (“EpiPath”) (to C.P.M.) and by a grant from the Ministry of Higher Education and Research of Luxembourg. V.K.S. was supported by the University of Luxembourg and by Luxembourg National Research Fund AFR PhD Fellowship 9825384. X.H. was supported by Deutsche Forschungsgemeinschaft Grant SCHA1067/3-1 (to H.S.). The funding bodies played no role in the writing of this manuscript, nor in the design, data collection, analysis, and interpretation of our data. J.D.T. is a management board member of the European Union–funded COST action CM1406.
Publisher Copyright:
Copyright © 2017 by The American Association of Immunologists, Inc. All rights reserved.
PY - 2017/12/15
Y1 - 2017/12/15
N2 - Early life adversity (ELA) has been associated with an increased risk for diseases in which the immune system plays a critical role. The ELA immune phenotype is characterized by inflammation, impaired cellular immunity, and immunosenescence. However, data on cell-specific immune effects are largely absent. Additionally, stress systems and health behaviors are altered in ELA, which may contribute to the generation of the ELA immune phenotype. The present investigation tested cell-specific immune differences in relationship to the ELA immune phenotype, altered stress parameters, and health behaviors in individuals with ELA (n = 42) and those without a history of ELA (control, n = 73). Relative number and activation status (CD25, CD69, HLA-DR, CD11a, CD11b) of monocytes, NK cells, B cells, T cells, and their main subsets were assessed by flow cytometry. ELAwas associated with significantly reduced numbers of CD69+CD8+ T cells (p = 0.022), increased numbers of HLA-DR+ CD4 and HLA-DR+ CD8 T cells (p < 0.001), as well as increased numbers of CD25+CD8+ T cells (p = 0.036). ELA also showed a trend toward higher numbers of CCR4+ CXCR32CCR6+ CD4 T cells. Taken together, our data suggest an elevated state of immune activation in ELA, in which particularly T cells are affected. Although several aspects of the ELA immune phenotype were related to increased activation markers, neither stress nor health-risk behaviors explained the observed group differences. Thus, the state of immune activation in ELA does not seem to be secondary to alterations in the stress system or health-risk behaviors, but rather a primary effect of early life programming on immune cells.
AB - Early life adversity (ELA) has been associated with an increased risk for diseases in which the immune system plays a critical role. The ELA immune phenotype is characterized by inflammation, impaired cellular immunity, and immunosenescence. However, data on cell-specific immune effects are largely absent. Additionally, stress systems and health behaviors are altered in ELA, which may contribute to the generation of the ELA immune phenotype. The present investigation tested cell-specific immune differences in relationship to the ELA immune phenotype, altered stress parameters, and health behaviors in individuals with ELA (n = 42) and those without a history of ELA (control, n = 73). Relative number and activation status (CD25, CD69, HLA-DR, CD11a, CD11b) of monocytes, NK cells, B cells, T cells, and their main subsets were assessed by flow cytometry. ELAwas associated with significantly reduced numbers of CD69+CD8+ T cells (p = 0.022), increased numbers of HLA-DR+ CD4 and HLA-DR+ CD8 T cells (p < 0.001), as well as increased numbers of CD25+CD8+ T cells (p = 0.036). ELA also showed a trend toward higher numbers of CCR4+ CXCR32CCR6+ CD4 T cells. Taken together, our data suggest an elevated state of immune activation in ELA, in which particularly T cells are affected. Although several aspects of the ELA immune phenotype were related to increased activation markers, neither stress nor health-risk behaviors explained the observed group differences. Thus, the state of immune activation in ELA does not seem to be secondary to alterations in the stress system or health-risk behaviors, but rather a primary effect of early life programming on immune cells.
UR - http://www.scopus.com/inward/record.url?scp=85038575408&partnerID=8YFLogxK
U2 - 10.4049/jimmunol.1701082
DO - 10.4049/jimmunol.1701082
M3 - Article
C2 - 29133294
AN - SCOPUS:85038575408
SN - 0022-1767
VL - 199
SP - 4046
EP - 4055
JO - Journal of Immunology
JF - Journal of Immunology
IS - 12
ER -